Disturbances in the balance of regional brain dopaminergic activity have been implicated in the symptomatology of schizophrenia. Recent studies in patients have led to the hypothesis that dysfunction in the dorsolateral prefrontal cortex (DLPFC) may cause the impaired motivation, shallow affect, and deficiencies in the performance of problem solving tasks suffered by schizophrenics. Analogous deficits are produced in primates by depletion of dopamine from the DLPFC. Together these observations suggest a role for DLPFC dopaminergic neurons in cognitive functions subserved by this area. Studies in rats have indicated that dopaminergic activity in the medial frontal cortex exerts a suppressive effect of dopaminergic activity in the striatum and nucleus accumbens. Weinberger has postulated that decreased dopaminergic activity in the DLPFC in schizophrenia may increase dopaminergic activity in striatum resulting in the positive features of schizophrenia. To determine whether a reciprocal relationship between prefrontal and sub-cortical dopaminergic activity exists in primates, dopamine was depleted in juvenile rhesus monkeys by local injections of 6-hydroxydopamine. Neurochemical analysis indicated that dopaminergic activity was increased in the putamen.